U p d a t e s i n t h e G e n e r a l A p p ro a c h

t o P e d i a t r i c H e a d Tr a u m a an d
Concussion
Shireen M. Atabaki, MD, MPH

KEYWORDS

Traumatic brain injury
Prediction rules
Computed tomography

Intracranial hemorrhage
Concussion

KEY POINTS

Head trauma and concussion are the cause of significant morbidity and mortality in child-
hood and are an important public health concern, increasing in incidence worldwide.

Acute recognition and management of traumatic brain injury along the spectrum from mild
to severe is essential in optimizing neurocognitive outcomes and preventing long-term
sequelae in children.

A thorough history and physical examination is the foundation for the acute diagnosis of
head trauma, and has recently been incorporated into validated risk stratification to
reduce unnecessary imaging and associated radiation and costs.

Knowledge translation and widespread dissemination of these prediction rules for pediat-
ric head trauma is the next step to obviate unnecessary computed tomography (CT) scans
in children.

Children with blunt head trauma and normal cranial CT results generally do not require
hospitalization for neurologic observation.

INTRODUCTION

A 12-year-old boy is brought into the Emergency Department (ED) of the local commu-
nity hospital by ambulance, following a rollover motor vehicle collision. The patient had
a brief loss of consciousness and presents with mild headache and amnesia for the
event. Emergency physicians order a computed tomography (CT) scan of the head.
The head CT is normal, and the patient is discharged home and told to follow up
with his pediatrician. One week later the child returns to school and complains of
headache while playing basketball; he is removed from the field and brought to the
ED by his parents, where a decision is made to obtain a head CT to rule out intracranial

Division of Emergency Medicine, Department of Pediatrics and Emergency Medicine, Children’s

National Medical Center, 111 Michigan Avenue Northwest, Washington, DC 20010-1970, USA
E-mail address: satabaki@cnmc.org

Pediatr Clin N Am 60 (2013) 1107–1122

http://dx.doi.org/10.1016/j.pcl.2013.06.001 pediatric.theclinics.com
0031-3955/13/$ – see front matter Ó 2013 Elsevier Inc. All rights reserved.
1108 Atabaki

hemorrhage. The scenario described is not uncommon, despite emerging evidence

and guidelines for imaging and concussion management for children with head
trauma.
Traumatic brain injury (TBI) is an important public health concern in children. There
are 1.4 million patients with TBI evaluated and discharged from EDs annually in the
United States.1 Of these, nearly half are children or young adults younger than
19 years.1 This figure may represent the tip of the iceberg, as it is believed that up
to 5 million patients incur TBI that is often neither recognized nor treated. The head
is the most frequently injured area in a child, and the most common causes of TBI
in the pediatric population are falls and motor vehicle collisions.1,2 TBI is also the
most common cause of death following childhood injury. Football is the most common
sport associated with TBI and with more than 1 million football players in the United
States, many of whom are high school and collegiate players, it has evolved into an
important area of national focus.3 Emergency physicians have become astute in the
diagnosis of severe and moderate TBI. However, as described in the vignette for
the 12-year-old patient, the evaluation and management of mild TBI (mTBI) is an
area in need of knowledge translation.
This article discusses the general approach to pediatric head trauma, skull fracture,
and TBI along the continuum from mild to severe. The focus is on updates to diag-
nostic and management modalities, including some of the most recent evidence-
based medicine guidelines and research. The article begins with mTBI, as this is the
area harboring the most advances in recognition and management.

CONCUSSION/MILD TBI
Description
The Centers for Disease Control and Prevention (CDC) use the term mTBI, which ac-
counts for 88% to 92% of cases of TBI, interchangeably with the term concussion.

mTBI or concussion is defined as a complex pathophysiologic process affecting

the brain, induced by traumatic biomechanical forces secondary to direct or indi-
rect forces to the head. mTBI is caused by a blow or jolt to the head that disrupts
the function of the brain. mTBI results in a constellation of physical, cognitive,
emotional and sleep-related symptoms. Duration of symptoms is variable and
may last as long as several days, weeks, months or even longer in some cases.4

This disturbance of brain function is typically associated with neurometabolic

dysfunction with normal structural anatomy. The neurometabolic cascade following
concussion consists of calcium influx, increase in glucose consumption, and
increased metabolic demand.5
Concussion can result in a variety of physical, cognitive, emotional, and sleep-
related symptoms lasting from days to months. Table 1 lists these symptoms,
including those most concerning, such as depression and anxiety. Unrecognized
and poorly managed concussion can result in postconcussion syndrome, with dura-
tion of symptoms lasting beyond 2 weeks and up to several months.6 Research has
demonstrated promise in early intervention and a program of graduated return to
play, sport, and school work for youth with concussion.7–9
Evaluation
The history and physical examination is the cornerstone of the diagnosis of concus-
sion. Psychometrically validated concussion-screening tools based on the history
and physical examination such as the Acute Concussion Evaluation (ACE) are effec-
tive, and have been coupled with management or “concussion care plans” available
 Pediatric Head Trauma 1109

Table 1
Concussion symptom checklist

Physical Cognitive Emotional Sleep

Headache Feeling mentally foggy Irritability Drowsiness
Nausea Feeling slowed down Sadness Sleeping less than usual
Vomiting Difficulty concentrating More emotional Sleeping more than usual
Balance problems Difficulty remembering Nervousness Trouble falling asleep
Dizziness
Visual problems
Fatigue
Sensitivity to light
Sensitivity to noise
Numbness
Tingling

Adapted from Centers for Disease Control and Prevention. Heads up: brain injury in your practice.
Available at: http://www.cdc.gov/concussion/HeadsUp/physicians_tool_kit.html.

as head injury toolkits on the CDC Web site at http://www.cdc.gov/concussion/

HeadsUp/physicians_tool_kit.html.4 A recent study found that very few EDs use any
form of concussion screening in the evaluation of pediatric head trauma.10 It was
noted that very few of the EDs surveyed had adequate patient education for the man-
agement of concussion. The CDC has established an effective Web site to make these
concussion toolkits available to physicians, patients, parents, school personnel, and
coaches,4 and has supported the work of investigators to adapt a previously psycho-
metrically validated concussion-screening tool (the ACE) for use in the ED as the
ACE-ED.10 Current work is ongoing to incorporate these concussion-screening tools
into the electronic health record and normal workflow to initiate assessment of chil-
dren with head trauma at the time of triage.

Sports Concussion
There are 1.1 million high school football players in the United States each year, of
whom nearly 70,000 are diagnosed with concussion.11 However, it is widely believed
that concussion is more prevalent in high school football. McCrea and colleagues12
found that although 30% of high school football players stated that they had a previ-
ous history of concussion, fewer than half had reported the injury. Reasons for failure
to report concussions included lack of awareness that a concussion had been sus-
tained and lack of understanding of the potentially serious nature of injury.
Recent media attention has focused on the fact that high school football players
may be reluctant to report concussion because of fear of being removed from compe-
tition13 and loss of athletic scholarships http://www.npr.org/2012/08/07/158361384/
love-of-sports-can-start-early-so-can-injuries.
Education of student athletes and parents on the impact of unrecognized and poorly
managed concussion is extremely valuable, and should be a discussion the medical
provider initiates at the time of the acute evaluation in the ED, at school, or on the field.

Legislation and Return-to-Play

Since 2009, 43 states and the District of Columbia have implemented legislation for
concussion management in youth athletics with established return-to-play guidelines.
If a student athlete is suspected to have a concussion, the athlete is removed from
play and requires clearance, in most cases from a licensed medical professional, to
1110 Atabaki

return to play. The recommendation is for those on the sidelines such as coaches and
athletic trainers to pull a child from the field when concussion is suspected and to have
the player “sit it out, if in doubt.” The reasons for this proactive removal from play are
to:

Allow for healing

Prevent “second-impact syndrome,” a serious diffuse axonal injury resulting in
uncal herniation14

Prevent neurocognitive sequelae of reinjury15
In addition to restrictions on physical activity, both the American Academy of Pedi-
atrics and Zurich Consensus Statement on Concussion in Sport recommend limitation
of scholastic and other cognitive activities for athletes following concussion
(Table 2).16,17
In addition, concussed players who continue to play are at increased risk of reinjury,
have delayed symptom onset, and neuropsychological deficits.18,19
Whereas prior return-to-play guidelines for concussion were based on static mea-
sures such as duration of loss of consciousness, current stepwise recommendations
for return to play are individualized and include17:

Resolution of symptoms

Return to baseline neurocognitive function
Subconcussive Injury
Talavage and colleagues19 were the first to present evidence of subconcussive injury
in a cohort of high school football players. This prospective study using head-impact
telemetry, neurocognitive testing, and functional magnetic resonance imaging uncov-
ered functionally detected cognitive impairment in high school football players with re-
petitive head trauma, without clinically diagnosed concussion. This finding raises
concern for athletes who suffer subconcussive impact, and highlights the need for
safety regulations in high-impact sports.

Table 2
Return-to-play guidelines for pediatric sport concussion

Restrictions Return to Play

Physical rest No sports Clearance by Licensed Independent
No weight training Practitioner (LIP) or concussion expert
No cardiovascular training If symptom-free at rest and exertion
No Physical Education Pass neurocognitive and balance
No bike riding assessment
Cognitive rest No homework Able to complete symptom-limited
Shortened school day exercise program
No reading No same-day return to play!
No video games, computers, cell
phones, or texting
No television
No travel
Increased rest and sleep

Immediate removal of athlete from play recommended if any sign or symptom of concussion is
witnessed.
Adapted from The Zurich Consensus Statement, an international conference of concussion
experts, McCrory P, Meeuwisse, Aubry M, et al. Consensus statement on concussion in sport: the
4th International Conference on Concussion in Sport held in Zurich, November 2012. Br J Sports
Med 2013;47:250–8; with permission.
 Pediatric Head Trauma 1111

Changes in Sports Regulation and Techniques

Student athletes participating in collision sports such as football may have as many
as 2000 impacts to the head during the course of an athletic season. This fact is of
particular concern, as high school football players appear to be more vulnerable
and perform worse than collegiate athletes following concussion. Protracted recov-
ery in high school players with concussion included prolonged memory dysfunction
and worse performance on neuropsychological testing when compared with
controls.20
Helmets and mouth guards have not been shown to decrease rates of concussion,
although helmets are effective in preventing skull fracture and more severe TBI.21
Ongoing research is aimed at understanding the mechanisms of injury and types of
play most likely to result in head trauma during sport. Improving techniques for play
and establishing regulation can decrease the rates of both head impact and
concussion.

Chronic Traumatic Encephalopathy

The postmortem neuropathologic studies of McKee and colleagues22 on chronic trau-
matic encephalopathy (CTE) resulting from repetitive head trauma have gained wide-
spread media attention. Blinded to the patient’s clinical history, McKee and
colleagues22 have documented CTE and associated neuropathologic changes with
tau-immunoreactive neurofibrillary tangles in the cortex, resulting in a progressive motor
neuron disease. These changes have been noted in a series of professional and youth
athletes and a host of others who have suffered repetitive head trauma. Table 3 lists
some of the neuropathologic findings and symptoms associated with CTE.23

Imaging
Nearly 700,000 children visit the ED for head trauma in the United States each year,
most with mTBI.1 More than 300,000 cranial CTs are obtained to evaluate these chil-
dren. Overall, a great deal of variation in practice exists in evaluation of mTBI with
cranial CT. In addition, CT is not without associated cost and risk. Research on
CT-radiation risk and extrapolated data from World War II atomic bomb survivors es-
timates that lifetime-attributable mortality from a single CT of the head in childhood is
as high as 1 in 1200.24 More recently, Pearce and colleagues25 discovered a 3-fold in-
crease in the risk of brain tumors following head CT (cumulative doses of 50–60 mGy
to the brain). The study linked CT records for patients (birth to 22 years of age) in the

Table 3
Neuropathologic findings and symptoms associated with chronic traumatic encephalopathy

Neuropathologic Changes Symptoms

Decreased brain mass Depression/apathy
Enlarged lateral and third ventricles Suicidal behavior
Brain atrophy Problems with executive function
Neurofibrillary tangles Problems with short term memory
b-Amyloid deposits Emotionally labile
Pallor Problems with impulse control

Adapted from Stern RA, Riley DO, Daneshvar DH, et al. Long-term consequences of repetitive brain
trauma: chronic traumatic encephalopathy. Phys Med Rehabil 2011;3:S460–7; with permission.
1112 Atabaki

British National Health Service to cancer registry data, and also found head CT to be
the most common scan obtained in this cohort.
More than a decade ago, the National Cancer Institute and Food and Drug Admin-
istration disseminated a guide to physicians to minimize unnecessary CT scans in chil-
dren.26,27 Despite this work, there was a dramatic increase in the use of CT scans for
children over the past 2 decades.28

Prediction Rules for Cranial CT after Head Trauma

In 2009, the Pediatric Emergency Care Applied Research Network (PECARN)29 pub-
lished 2 validated prediction rules to identify children at very low risk of clinically impor-
tant TBI (ciTBI), not in need of a CT scan.30 More than 40,000 children 0 to 18 years of
age were prospectively enrolled in the PECARN study. Table 4 lists the two prediction
rules, one for preverbal children (<2 years) and the other for verbal children (2 years).
The PECARN prediction rules have excellent performance characteristics, and were
derived by incorporating clinical findings that were readily available and had good
interobserver reliability.31 If none of the 6 predictors in either prediction rule is present,
the child is at very low risk of ciTBI, and CT can be avoided.
For children younger than 2 years the prediction rule had:

Negative predictive value of 100% (95% confidence interval [CI] 99.7–100.0)

Sensitivity of 100% (95% CI 86.3–100.0)
For children 2 years and older the prediction rule had:

Negative predictive value of 99.95% (95%CI 99.81–99.99)

Sensitivity of 96.8% (95% CI 89.0–99.6)
ciTBI, the outcome of interest, was defined as:

Death from TBI

Neurosurgical intervention for TBI

Table 4
PECARN prediction rule for clinically important TBI (ciTBI) in children younger than 2 and in
those 2 years and older

PECARN Prediction Rule for <2 y PECARN Prediction Rule for ‡2 y

GCS <15 GCS <15
Sign of altered mental status Signs of altered mental status
Palpable skull fracture Signs of basilar skull fracture
Occipital, parietal, or temporal scalp hematoma Severe headache
History of LOC 5 s History of LOC
Severe mechanism of injurya Severe mechanism of injurya
Not acting normally per parent History of vomiting

If patients have no sign or symptom in the prediction rule, CT scan is not recommended as they are
at very low risk of ciTBI.
Abbreviations: GCS, Glasgow Coma Scale score; LOC, loss of consciousness.
a
Severe mechanism of injury: motor vehicle crash with patient ejection, death of another pas-
senger, or rollover; pedestrian or bicyclist without helmet struck by a motorized vehicle; falls more
than 0.9 m (3 feet) for <2 years or more than 1.5 m (5 feet) for 2 years; head struck by a high-
impact object.
Data from Kuppermann N, Holmes JF, Dayan PS, et al, for the Pediatric Emergency Care Applied
Research Network (PECARN). Identification of children at very low risk of clinically-important brain
injuries after head trauma: a prospective cohort study. Lancet 2009;374:1160–70.
 Pediatric Head Trauma 1113

Intubation longer than 24 hours

Hospitalization 2 nights or longer for TBI; with TBI on CT
The PECARN study risk stratifies children with minor head trauma into high risk, in-
termediate risk, and low risk, for clinically important TBI (Fig. 1). This risk stratification
provides the Emergency Physician with easy-to-use recommendations for CT

A
GCS=14 or other signs of altered mental status†,
Yes
CT recommended
or palpable skull fracture 13.9% of population
4.4% risk of ciTBI

No

Occipital or parietal or temporal scalp haematoma, Yes Observation versus CT on the basis
or history of LOC ≥5 s, or severe mechanism of of other clinical factors including:
injury‡, or not acting normally per parent 32.6% of population • Physician experience
0.9% risk of ciTBI • Multiple versus isolated§ findings
• Worsening symptoms or signs after
53.5% of population
No emergency department observation
<0.02% risk of ciTBI
• Age <3 months
• Parental preference
CT not recommended¶

B
GCS=14 or other signs of altered mental status†,
Yes
CT recommended
or signs of basilar skull fracture 14.0% of population
4.3% risk of ciTBI

No

History of LOC, or history of vomiting, or severe Yes Observation versus CT on the basis
mechanism of injury‡, or severe headache of other clinical factors including:
27.7% of population • Physician experience
0.9% risk of ciTBI • Multiple versus isolated§ findings
58.3% of population • Worsening symptoms or signs after
No
<0.05% risk of ciTBI emergency department observation
• Parental preference
CT not recommended¶
Fig. 1. Suggested computed tomography (CT) algorithm for children younger than 2 years
(A) and for those aged 2 years and older (B) with Glasgow Coma Scale (GCS) scores of
14 to 15 after head trauma (Data are from the combined derivation and validation popula-
tions). ciTBI, clinically important traumatic brain injury; LOC, loss of consciousness. y Other
signs of altered mental status: agitation, somnolence, repetitive questioning, or slow
response to verbal communication; z Severe mechanism of injury: motor vehicle crash with
patient ejection, death of another passenger, or rollover; pedestrian or bicyclist without
helmet struck by a motorised vehicle; falls of more than 0.9 m (3 feet) (or more than 1.5 m
[5 feet] for panel B); or head struck by a high-impact object; x Patients with certain isolated
findings (ie, with no other findings suggestive of traumatic brain injury), such as isolated
LOC, isolated headache, isolated vomiting, and certain types of isolated scalp haematomas
in infants older than 3 months, have a risk of ciTBI substantially lower than 1%; { Risk of ciTBI
exceedingly low, generally lower than risk of CT-induced malignancies. Therefore, CT scans
are not indicated for most patients in this group. (From Kuppermann N, Holmes JF, Dayan
PS, et al, for the Pediatric Emergency Care Applied Research Network (PECARN). Identifica-
tion of children at very low risk of clinically-important brain injuries after head trauma: a
prospective cohort study. Lancet 2009;374:1160–70; with permission.)
1114 Atabaki

decision making. For the low-risk group CT is not recommended, and for the high-risk
group (those with altered mental status, Glasgow Coma Scale [GCS] <15 or signs of
skull fracture) CT is recommended. For the intermediate-risk group, for whom obser-
vation is recommended versus CT scan, observation often provides a reasonable
alternative to cranial CT in the evaluation of the child with minor TBI. This finding holds
particularly true for children with isolated predictors, such as isolated loss of con-
sciousness,32 isolated headache, or vomiting,33,34 who have a low risk of ciTBI. In a
secondary analysis of the PECARN cohort, with clinical observation periods docu-
mented to be 3 to 6 hours, investigators found that clinical observation was associated
with reduced CT use.
Application of the PECARN prediction rules in general EDs, where the majority of
children with head trauma are evaluated and CT scan rates are close to 50%, could
result in a significant reduction in unnecessary scans.

Hospitalization
Children with minor blunt head trauma seen in the ED frequently undergo CT, and are
hospitalized for observation and serial neurologic examinations. These children may at
times also receive subsequent CT scans. Children with blunt head trauma and normal
cranial CT results generally do not require hospitalization for neurologic observation.
Holmes and colleagues35 found that of approximately 14,000 children with minor blunt
head trauma (GCS 14 or 15) and normal ED CT scans, nearly one-fifth were hospital-
ized and 2% had subsequent neuroimaging, although none required neurosurgical
intervention.
Table 5 summarizes new developments in the management of pediatric head
trauma.

MODERATE AND SEVERE TBI

TBI is the leading cause of morbidity and mortality in children. The incidence of TBI has
increased worldwide, most likely as a result of increased automobile use. The World
Health Organization (WHO) projects that mortality from TBI related to road traffic ac-
cidents will double over a 2-decade period from 2000 to 2020.36

Table 5
What’s new in the management of pediatric head trauma

Issue Recommendation Reference

CT Validated PECARN prediction rules based on Kuppermann et al,30 2009
signs and symptoms can identify children
with head trauma at very low risk of
clinically important TBI in whom CT is not
recommended
Repeat CT Children with minor blunt head trauma and Holmes et al,35 2011
initial normal cranial CT generally do not
warrant subsequent CT
Hospitalization Children with minor blunt head trauma and Holmes et al,35 2011
normal cranial CT results generally do not
require hospitalization for neurologic
observation

From Kuppermann N, Holmes JF, Dayan PS, et al, for the Pediatric Emergency Care Applied Research
Network (PECARN). Identification of children at very low risk of clinically-important brain injuries
after head trauma: a prospective cohort study. Lancet 2009;374:1160–70; with permission.
 Pediatric Head Trauma 1115

It is essential to assess the pedestrian struck by an automobile for head trauma, as

demonstrated in Waddell’s triad (Fig. 2).38
Head trauma resulting in neuronal injury in moderate or severe TBI follows a
biphasic pattern:

Primary injury
 Acute

Secondary injury
 May occur hours to days after head trauma
 Indirect injury resulting from
- Hypoxemia

- Hypotension

- Cerebral edema

- Hypoglycemia

Early initiation of therapy and the use of standardized guidelines in the manage-
ment of moderate and severe TBI are essential to improve outcomes in children.
However, randomized controlled trials in children with moderate and severe TBI
are rare and children and are often excluded from large randomized controlled trials
in adults.
Prehospital care for severe TBI has not changed in the past decade, and focuses on:

The management of ABCs (Airway, Breathing, Circulation)
 Patient with GCS less than 9 should be intubated via rapid-sequence
intubation
 Ketamine is contraindicated, as it can increase intracranial pressure (ICP)

Triage to a trauma center
 Based on GCS
 Signs of ICP, Cushing’s triad, unequal pupils
 Higher survival in severe TBI for patients directly transported by emergency
medical services to a pediatric trauma center39
 Reduced mortality in subdural hematoma if operated within 4 hours after
injury40

Fig. 2. Waddell’s triad37 demonstrates a pedestrian child struck by an automobile. The child
is hit on the left side with bumper impact to the femur and fender impact to the abdomen,
then is thrown to the ground with impact to the head. (From Atabaki SM. Prehospital eval-
uation and management of traumatic brain injury in children. Clin Pediatr Emerg Med
2006;7:94–104; with permission.)
1116 Atabaki

Prevention and treatment of hypoxemia41

 Brain injury can lead to respiratory depression and failure

Treatment of hypotension
 Fluid resuscitation
 Maintain systolic blood pressure higher than 70 1 (2  age in years)
42
- Prehospital initiation of treatment of hypotension improves outcomes
43
- Hypotension is a sensitive indicator of mortality

 Treatment of hypoglycemia44
- Glucose should be checked

- TBI induces increased energy demands and hyperglycolysis

In 2012, the Brain Trauma Foundation published guidelines for the acute medical
management of severe TBI in children, based on a review of the literature. Levels
were given on a scale of I (highest) to III (lowest) for recommendations based on the
strength of the underlying research (Table 6).45
Indications for hypertonic saline or mannitol and hyperventilation include signs of
increased ICP or cerebral herniation such as:

Cushing’s triad
 Triad of hypertension, bradycardia, and irregular respirations

Abnormal pupil examination
 Asymmetric, fixed, or dilated pupils

Neurologic deterioration
 Drop in GCS greater than 2 points for patients with GCS less than 953

Posturing
 Extensor posturing

Table 6
Select therapies for moderate or severe TBI

Reference
Therapy Recommended
Hyperosmolar therapy Peterson et al,46 2000
Effective to control increased ICP in severe TBI Simma et al,47 1998
Hypertonic 3% saline 0.1–1 mL/kg/h Fisher et al,48 1992
Mannitol 0.25–1 g/kg
Level III recommendation
Temperature control Adelson et al,49 2005
Hyperthermia should be avoided in severe TBI Hutchison et al,50 2008
Moderate hypothermia (32–33 C) may be considered
in severe TBI
Level III recommendation
Therapy Not Recommended
Hyperventilation Curry et al,51 2008
Prophylactic hyperventilation to be avoided
Level III recommendation
Corticosteroids Fanconi et al,52 1988
Corticosteroids should be avoided in severe TBI
Level III recommendation

Adapted from Kochanek PM, Carney N, Adelson PD, et al. Guidelines for the acute medical man-
agement of severe traumatic brain injury in infants, children and adolescents-second edition.
Pediatr Crit Care Med 2012;13:S1–82; with permission.
 Pediatric Head Trauma 1117

Prophylaxis of Posttraumatic Seizure

Head trauma is the cause of 5% of epilepsy in children and is the cause of 20,000 new
cases of epilepsy each year.54 Nearly 20% of patients with severe TBI will develop
posttraumatic epilepsy (PTE).54,55 Prior trials of phenytoin, carbamazepine, and val-
proate to prevent PTE in animal models and humans have not been successful.56,57
However, prophylaxis with phenytoin to prevent early posttraumatic seizure may be
considered.
Levetiracetam has emerged as a promising therapy to prevent PTE. Levetiracetam
has been effective in animal models in preventing PTE and is used in humans to treat
nontraumatic epilepsy.58 Recently published studies on the safety and pharmacoki-
netics of levetiracetam in children with severe TBI and intracranial hemorrhages
pave the way for future randomized controlled trials.59,60
Intraventricular Hemorrhage
Children with isolated intraventricular hemorrhage (IVH) have better outcomes than
those with combination of IVH and other intracranial injury on CT (nonisolated IVH).
Lichenstein and colleagues61 report that of approximately 15,000 children with CT
for head trauma, 7% had intracranial injury and 0.9% had isolated IVH. This isolated
IVH group had good outcomes; none required neurosurgery or died. By contrast, of
37% of patients with nonisolated IVH, 37% died and 42% required neurosurgery.
Skull Fractures
Head trauma in younger children often results in skull fracture, which may also be
associated with an underlying intracranial injury. If skull fracture is suspected to result
from a hematoma in the presence of underlying bony step-off or significant tenderness
of the skull, and intracranial injury is also suspected, a cranial CT scan is warranted.
Signs of skull fracture place children at higher risk of ciTBI, and a CT scan is often rec-
ommended in this population to uncover underlying intracranial disorder. In general,
the majority of skull fractures are linear and are associated with good outcomes.
Basilar Skull Fracture
If a basilar skull fracture is suspected a CT scan should be obtained, owing to the poor
sensitivity of plain radiography in detecting these injuries. Patients with identified

Fig. 3. Signs of a basilar skull fracture in a patient with head trauma include raccoon eyes
and Battle sign. (From Atabaki SM. Prehospital evaluation and management of traumatic
brain injury in children. Clin Pediatr Emerg Med 2006;7:94–104; with permission.)
1118 Atabaki

basilar skull fractures are no longer routinely hospitalized, and can be closely
observed by guardians as outpatients. The routine administration of prophylactic anti-
biotic is also no longer recommended. However, these children should be closely
observed for signs of intracranial infection, and told to return for immediate medical
attention if they develop a fever or neurologic deficit, especially within the first few
weeks following head trauma (Fig. 3).

SUMMARY

Head trauma and concussion are the cause of significant morbidity and mortality in
childhood and are an important public health concern, increasing in incidence
worldwide. Acute recognition and management of TBI along the spectrum from
mild to severe is essential to optimize neurocognitive outcomes and prevent
long-term sequelae in children. A thorough history and physical examination is
the foundation for the acute diagnosis of head trauma, and has recently been incor-
porated into validated risk stratification to reduce unnecessary imaging and asso-
ciated radiation and costs. Knowledge translation and widespread dissemination
of these prediction rules for pediatric head trauma is the next step to obviate un-
necessary CT scans in children. In addition, children with blunt head trauma and
normal cranial CT results generally do not require hospitalization for neurologic
observation.
Concussion is common following head trauma in children, and resulting symptoms
can last for months if not diagnosed and managed properly. Postconcussive symp-
toms such as depression, anxiety, and difficulty with executive function can have a
profound impact during vulnerable periods in a child’s life. Emerging evidence and
expert consensus demonstrate a program of cognitive and physical-activity manage-
ment with a graduated program of return to play, sport, and school to be effective in
improving outcomes following concussion. Over the last decade, “Return to Play”
legislation for youth has been adopted by most states. There has also been an
increased awareness of the long-term neurocognitive effects of concussion among
professional and collegiate athletes. Now more than ever it is essential for health
care providers to expand the latest research in concussion to the acute care of pedi-
atric head trauma.
Outcomes of patients with head trauma have improved greatly, with a 20% drop in
mortality rates from TBI over the last 30 years. The management of moderate and se-
vere TBI in children is still an area of many unknowns; however, appropriate triage and
systemic resuscitation to prevent and treat hypoxemia and hypotension have been
effective in improving outcomes. Following standardized guidelines for the triage
and management of children with severe TBI will pave the way for future trials of ther-
apeutic interventions for moderate and severe pediatric TBI.

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